During the past year we have demonstrated that immune privilege within the anterior chamber of the eye is a dynamic, specific process in which both transplantation and tumor-specific cellular immune mechanisms are systemically suppressed while humoral immune functions remain intact. We refer to this process as anterior chamber-associated immune deviation (ACAID) and have shown that its induction and maintenance require a functional intact spleen. Our goals for the ongoing research include: (1) Identify and analyze the splenic cellular components that promote ACAID; (2) Determine if ACAID can be transferred with serum (blocking factors) or cells (suppressor cells); (3) Determine if ACAID-like processes can be induced by injecting allogeneic cells via other routes (e.g. intracranial, intratesticular, or i.v.); (4) Determine if ACAID can be induced by intracameral injection of allogeneic lymphoid cells; (5) Develop additional models of ACAID by employing different tumor cell lines and inbred mouse strains.